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Schwann Cell Options for chronic Pain Eradication

Project description

Insight into the mechanism of chronic pain

Peripheral sensory neurons in the skin known as nociceptors alert us to potentially damaging stimuli by detecting signals or responding to chemicals from damaged tissue. Nociceptors transform these stimuli into electrical signals in the brain, causing the sensation of pain. The EU-funded SCOPE project aims to address the limited efficacy of existing analgesic medications against chronic pain associated with cancer and central neuropathies. Researchers will focus on the transient receptor potential ankyrin 1 (TRPA1) channel, which is expressed in Schwann cells and is implicated in acute pain. The idea is to investigate the role of the TRPA1–Schwann cell axis in chronic pain and identify putative new drug targets.

Objective

Chronic pain, characterized by increased sensitivity to innocuous/mild stimuli (allodynia), afflicts 25% of the European adult population. Efficacy and/or safety of analgesic medicines is limited, and the treatment of chronic pain associated with inflammation, peripheral and central neuropathies and cancer remains unsatisfactory. Thus, identification of novel targets for better and safer analgesics is a major medical need. Transient receptor potential ankyrin 1 (TRPA1) channel, expressed by a subpopulation of primary sensory neurons (nociceptors), has been proposed as a major transducer of acute pain. We have, recently, identified that TRPA1 is expressed in Schwann cells that ensheath peripheral nerve fibres. In a prototypical model of neuropathic pain (sciatic nerve ligation in mice), we discovered that Schwann cell-TRPA1 exerts a hitherto unknown role that, via amplification of the oxidative stress message, sustains neuroinflammation and chronic pain (allodynia). Thus, Schwann cells, through their own repertoire of channels and enzymes orchestrate in the injured/inflamed tissue an autocrine/paracrine signalling pathway to sustain chronic pain. The purpose of the present project is to extend this observation to other models of inflammatory, neuropathic and cancer pain to identify a general paradigm based on Schwann cell/TRPA1/oxidative stress as the pathway that sustains chronic pain. We aim also at identifying in oligodendrocytes (the Schwann cells of the brain) whether the TRPA1/oxidative stress pathway sustains pain in the central nervous system. In mouse, rat and human Schwann cells/oligodendrocytes we aim at identifying biomarkers and combine them into biosignatures predictive of the susceptibility to the development of chronic pain. We anticipate that each molecular step that entails the TRPA1/oxidative stress pathway in Schwann cell lineages is an eligible target for discovering new effective and safer medicines for the treatment of chronic pain.

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Topic(s)

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ERC-ADG - Advanced Grant

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Call for proposal

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(opens in new window) ERC-2018-ADG

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Host institution

UNIVERSITA DEGLI STUDI DI FIRENZE
Net EU contribution

Net EU financial contribution. The sum of money that the participant receives, deducted by the EU contribution to its linked third party. It considers the distribution of the EU financial contribution between direct beneficiaries of the project and other types of participants, like third-party participants.

€ 2 185 921,00
Address
Piazza San Marco 4
50121 Florence
Italy

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Region
Centro (IT) Toscana Firenze
Activity type
Higher or Secondary Education Establishments
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Total cost

The total costs incurred by this organisation to participate in the project, including direct and indirect costs. This amount is a subset of the overall project budget.

€ 2 185 921,00

Beneficiaries (1)

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